Patients with systemic lupus erythematosus (SLE) appear to have an increased susceptibility to infections caused by pyogenic organisms. In order to determine the pathogenesis of this major cause of morbidity and mortality, the applicant proposes to examine the functions in vitro of two major components of host defenses in patients with SLE: polymorphonuclear leukocytes (PMN) and the complement system. Specific attention will be directed at humoral and cellular aspects of chemotoxis, the function of PMN cell surface receptors for immunoglobulins and complement, and opsonic activity attributable to the alternative pathway of complement activation. With regard to the first of these, the applicant will explore the nature and mechanism of action of an inhibitor of complement (C5)-derived chemotactic activity found in SLE serum. Abnormal function of PMN and complement in patents with SLE will be related to disease activity, therapy and several serologic parameters (e.G., antinuclear antibodies, complement levels, antibodies to DNA, etc.). These studies should provide important new information regarding host defense mechanisms in SLE.